Autonomic Nervous System NUR 730 2024 PDF

The Autonomic Nervous System STACEY SCHLESINGER, DNP, MBA, CRNA Cervical Ganglia Cervical ganglia provide sympathetic innervation to head, neck, arms, and upper chest Cervical ganglia are divided into superior, medial and inferior cervical ganglia Inferior cervical ganglion...

The Autonomic Nervous System STACEY SCHLESINGER, DNP, MBA, CRNA Cervical Ganglia Cervical ganglia provide sympathetic innervation to head, neck, arms, and upper chest Cervical ganglia are divided into superior, medial and inferior cervical ganglia Inferior cervical ganglion fuses with 1st thoracic ganglion in 80% of individuals to form the Stellate Ganglion (aka Cervicothoracic ganglion) Stellate ganglion blocks are used to treat chronic regional pain syndromes, craniofacial hyperhidrosis, refractory angina, postherpetic neuralgia, PTSD, PVD, and long -Covid Horner’s Syndrome: ptosis, miosis and anhidrosis  SNS and PSNS Nerve Fibers Preganglionic nerve fibers are: MYELINATED Diameters < 3 mm Conduction velocity 3-15 m/sec Postganglionic nerve fibers are: UNMYELINATED Conduction velocity 2 m/sec (SLOW!) Physiologic Anatomy of ANS SNS and PSNS are the efferent (motor) component of the ANS Most organs receive fibers from both divisions Exceptions: Sweat glands are innervated by only SNS fibers 2-Neuron System Two-neuron (bipolar) chain from the CNS to the effector organ Preganglionic Neuron Postganglionic Neuron Receptors on Effector Organs Acetylcholine, norepinephrine, epinephrine are secreted from autonomic nerve ending Requires binding with specific receptors on effector cells Binding causes a conformational change → excitation or inhibition Opens or closes ion channel → alters permeability of cell membrane to various ions Second messenger enzymes → Activation or inactivation of enzyme on interior of cell SNS and PSNS Neurotransmitters Cholinergic = Acetylcholine Adrenergic = Norepinephrine ALL PREGANGLIONIC NERVE FIBERS in BOTH SNS and PNS are CHOLINERGIC (secrete acetylcholine) ALMOST ALL PARASYMPATHETIC POSTGANGLIONIC NERVE FIBERS are CHOLINERGIC (secrete acetylcholine) MOST SYMPATHETIC POSTGANGLIONIC NERVE FIBERS are ADRENERGIC (secrete norepinephrine) Acetylcholine and Norepinephrine Synthesis Acetylcholine Synthesis Brainstuff.org Norepinephrine Synthesis Sciencedirect.com Norepinephrine and Epinephrine Metabolism Source: APEX Cholinergic Receptors Acetylcholine activates both muscarinic & nicotinic receptors Muscarinic receptors are found on all effector cells that are stimulated by postganglionic cholinergic neurons of either the PSNS or SNS Nicotinic receptors are found in the autonomic ganglia at the synapses between the preganglionic and postganglionic neurons of both SNS and PSNS. Nicotinic receptors are also found outside the ANS (NMJ) Cholinergic Receptors  Adrenergic Receptors Alpha receptor activation: Activation of alpha receptors can cause excitation or inhibition Vasoconstriction, iris dilation, intestinal relaxation, intestinal sphincter contraction, pilomotor contraction, blader sphincter contraction, inhibits neurotransmitter release Beta receptor activation: Activation of beta receptors can cause excitation or inhibition Vasodilation, cardioacceleration, increased contractility, intestinal relaxation, uterus relaxation, bronchodilation, calorigenesis, lipolysis, bladder wall relaxation, thermogenesis Norepinephrine and epinephrine activate both alpha & beta receptors Norepinephrine: works primarily on alpha receptors Epinephrine: works equally on both alpha and beta receptors Postganglionic Breakdown of Acetylcholine & Norepinephrine ACETYLCHOLINE: Acetylcholine is broken down into acetate and choline by the enzyme acetylcholinesterase Same as mechanism at neuromuscular junction Choline is “recycled” to make more acetylcholine NOREPINEPHRINE: Three mechanisms terminate activity of norepinephrine in seconds: 1. Active reuptake (50-80% of norepinephrine) 2. Diffusion away from nerve endings → body fluids and blood 3. Destruction by tissue enzymes Monoamine oxidase (found in nerve endings) Catechol-O-methyl transferase (found throughout tissues) Anesthesia = Managing the ANS Goal: Railroad Tracks! The Autonomic Nervous System (ANS) Controls BP, GI motility /secretion, bladder emptying, sweating temp Activated by centers in spinal cord, brainstem and hypothalamus Influenced also by limbic system (memory/ emotion/ fear) ANS can respond rapidly Can increase HR to 2x normal within 3-5 seconds Can increase BP to 2x normal in 10-15 secs Parasympathetic: “REST and DIGEST” or “FEED and BREED” Sympathetic: “FIGHT or FLIGHT” Homeostasis Between the PSNS and SNS Homeostasis Between the PSNS and SNS (continued) Higher Level Organization of the SNS Hypothalamus Long-term BP control Reactions to physical and emotional stress Sleep Sexual reflexes Medulla oblongata and pons “Momentary” hemodynamic adjustments Sequence and automaticity of ventilation Maintaining constant “tonicity” Nucleus tractus solitarius relays afferent chemoreceptor and baroreceptor for SNS response SNS (Thoracolumbar System) Originates in spinal cord (T1-L2) Preganglionic neuron lies in intermediolateral horn of spinal cord Passes through ventral root -> white ramus -> sympathetic chain ganglia Synapse with postganglionic neuron Postganglionic neuron originates in either sympathetic chain ganglia or peripheral sympathetic ganglia and transmits impulse to the effector organ Exception: adrenal medulla has only preganglionic fibers PSNS (Craniosacral System) Has preganglionic & postganglionic neurons Originate in brainstem and sacrum Also found in CN III, VII, IX and X III (oculomotor) VII (facial) IX (glossopharyngeal) X (vagus) Sacral outflow originates in intermediolateral gray horns of sacral nerves VAGUS NERVE (X) accounts for 75% of PSNS (Parasympathetic Nervous System) activity Parasympathetic and Sympathetic Tone Constant activity of SNS and PSNS maintain basal rate of activity Allows a single nervous system to both increase and decrease activity of a stimulated organ Sympathetic tone causes baseline blood vessel constriction Parasympathetic tone maintains baseline GI motility Adrenal medulla maintains basal secretion Epinephrine 0.2 mcg/kg/min Norepinephrine 0.05 mcg/kg/min Enough to maintain normal BP even if all direct innervation was removed  Adrenal Medulla Preganglionic sympathetic nerve fibers pass WITHOUT SYNAPSING from spinal cord-> through the sympathetic chain-> adrenal medulla Innervated by PREGANGLIONIC fibers that secrete EPINEPHRINE and NOREPINEPHRINE (not acetylcholine) Effects: same as sympathetic stimulation Prolonged DOA (5-10x) because they are removed slowly from the blood Organs are stimulated in two ways (SNS and adrenal medulla) Dual mechanism of sympathetic stimulation = safety Adrenal medulla also can stimulate structures that NOT innervated by direct sympathetic fibers! Sweat Glands SNS stimulation increases sweat production of sweat glands Sympathetic fibers to most sweat glands are CHOLINERGIC (acetylcholine) Exception: adrenergic fibers to palms and soles Autonomic Reflexes Baroreceptor Reflex: Stretch receptors in walls of major arteries (carotid artery, aortic arch) detect STRETCH “High Pressure” impulses are sent to the brain stem Sympathetic impulses inhibited/Parasympathetic impulses increase BP returns to normal Gastrointestinal Reflexes: Smell of food increases salivation and GI secretion of digestive juices Rectal Emptying Reflex /defecation Sexual Reflexes: Erection (parasympathetic) and ejaculation (sympathetic) Other Reflexes: Pancreatic secretion, gallbladder contraction, kidney excretion of urine, sweating, blood glucose concentration Denervation Injury Intrinsic compensation for denervation injury Intrinsic tone in smooth muscle of vessels increases following injury Chemical adaptations Increased sensitivity to circulating catecholamines Eventually restores almost normal vasoconstriction Parasympathetic compensation may require many months Denervation supersensitivity (upregulation) Can see enhanced effect of administered catecholamines  Autonomic Dysreflexia Condition that emerges after a spinal cord injury Usually above T6 level Dysregulation of ANS leads to an uncoordinated sympathetic response that may result in a potentially life-threatening hypertensive episode when there is a noxious stimulus below the level of the spinal cord injury Noxious stimuli consist usually of bladder or bowel distension The higher the injury, the greater the severity of CV dysfunction Significantly increased risk of stroke by 300% to 400% Autonomic Dysreflexia Autonomic Pharmacology: Drugs may be used to either mimic or block the action(s) of the autonomic nervous system Sympathomimetics (adrenergic agonists): mimic the action of catecholamines; increase SNS activity Cholinomimetics: mimic the effect of acetylcholine; increase PSNS activity Adrenergic Antagonists (adrenergic blockers): block the action of catecholamines; decrease SNS activity Anticholinergics: block the effect of acetylcholine, decrease PSNS activity Note: Drug effects depends on specific receptors affected! Note: need to know/ understand how the medication works (i.e. does it activate receptors directly? Increase release of naturally occurring neurotransmitters from storage vesicles? Alter the breakdown of the neurotransmitter Autonomic Pharmacology Sympathomimetics Adrenergic Antagonists Adrenergic antagonists prevent activation of adrenergic receptors Used to treat HTN, angina, BPH, migraine headaches Effect depends on adrenergic receptor type(s) Alpha-adrenergic blocking agents: Beta-adrenergic blocking agents: Examples: Selective Beta-1: atenolol, metoprolol, esmolol Nonselective: Beta-1 and Beta-2: Propranolol Beta-1, Beta-2 and alpha-1: Labatalol, Carvedilol ALL adrenergic antagonists produce reversible (competitive) blockade EXCEPT Cholinergics (Cholinomimetics) Cholinergic medications stimulate the PSNS Directly activate cholinergic receptors (acts like acetylcholine) OR Indirectly by preventing the breakdown of acetylcholine Two types of cholinergic receptors: muscarinic and nicotinic Muscarinic: brain, glands (i.e. salivary), smooth muscle (GI tract, GU) Nicotinic: autonomic ganglia, NMJ, adrenal medulla Remember: ANTICHOLINERGICS block the action of acetylcholine Decreases PSNS activity ANTICHOLINESTERASES block the action of acetylcholinesterase Increases PSNS activity Cholinergic Crisis Excessive muscarinic stimulation & depolarizing neuromuscular blockade Dumbels Diaphoresis/Diarrhea Urination Miosis Bradycardia/Bronchospasm/Bronchorrhea Emesis Lacrimation Salivation Sludge and the Killer Bs Salivation Lacrimation Urination Diaphoresis/Diarrhea Gastrointestinal cramping Emesis *Muscarinic (cholinergic) Bradycardia toxicity can be caused by Bronchospasm either muscarinic agonists or Bronchorrhea cholinesterase inhibitors. Questions?